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1. Ballen KK, Becker PS, Emmons RV, Fitzgerald TJ, Hsieh CC, Liu Q, Heyes C, Clark Y, Levy W, Lambert JF, Chiafari F, Szymanski I, Rososhansky S, Popovsky MA, Stewart FM, Quesenberry PJ: Low-dose total body irradiation followed by allogeneic lymphocyte infusion may induce remission in patients with refractory hematologic malignancy. Blood; 2002 Jul 15;100(2):442-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Low-dose total body irradiation followed by allogeneic lymphocyte infusion may induce remission in patients with refractory hematologic malignancy.
  • Allogeneic stem cell transplantation is curative for certain cancers, but the high doses of chemotherapy/radiotherapy lead to toxicity.
  • Here, we treat patients with refractory cancer with 100 cGy total body irradiation (TBI) followed by infusion of nonmobilized pheresed allogeneic peripheral blood cells.
  • Twenty-five patients, with a median age of 47 years, with refractory cancers were enrolled.
  • Twelve patients with hematologic malignancies were treated; 1 received a cord blood transplant and 11 received sibling donor cells.
  • The development of chimerism correlated with hematologic malignancy (P <.001), total previous myelotoxic chemotherapy (P <.001), T-cell dose (P =.03), and graft-versus-host disease (P =.01).
  • Engraftment was achieved in patients with hematologic malignancies who had been heavily pretreated, suggesting the degree of immunosuppression may be a determinant of engraftment.
  • Low-dose TBI and allogeneic lymphocyte infusion may induce remission in patients with refractory hematologic malignancy.
  • [MeSH-major] Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / methods. Lymphocyte Transfusion / methods. Whole-Body Irradiation / methods
  • [MeSH-minor] Adult. Aged. Fetal Blood. Graft Survival. Humans. Middle Aged. Radiation Dosage. Remission Induction / methods. Salvage Therapy. Transplantation Chimera. Transplantation Conditioning / adverse effects. Transplantation Conditioning / methods. Transplantation Conditioning / mortality. Treatment Outcome

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  • [CommentIn] Blood. 2003 Jan 1;101(1):373; author reply 373-4 [12485941.001]
  • (PMID = 12091334.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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2. Ballen KK, Colvin G, Porter D, Quesenberry PJ: Low dose total body irradiation followed by allogeneic lymphocyte infusion for refractory hematologic malignancy--an updated review. Leuk Lymphoma; 2004 May;45(5):905-10
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  • [Title] Low dose total body irradiation followed by allogeneic lymphocyte infusion for refractory hematologic malignancy--an updated review.
  • Allogeneic stem cell transplantation is curative for certain cancers, but the high doses of chemotherapy and radiotherapy used in conventional myeloablative conditioning regimens may lead to severe toxicity.
  • In our initial study, we treated 25 patients with refractory cancers with 100 cGy total body irradiation (TBI) followed by allogeneic, non mobilized peripheral blood cells.
  • Twelve patients with hematologic malignancies were treated, 1 received a cord blood transplant and 11 received sibling donor cells.
  • The development of chimerism correlated with total previous myelotoxic chemotherapy (p < 0.001).

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  • (PMID = 15291347.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA104092-01; United States / NCI NIH HHS / CA / CA104092-02; United States / NCI NIH HHS / CA / L30 CA104092-01; United States / NCI NIH HHS / CA / L30 CA104092-02
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD3
  • [Number-of-references] 39
  • [Other-IDs] NLM/ NIHMS23277; NLM/ PMC1986764
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3. Dey BR, McAfee S, Sackstein R, Colby C, Saidman S, Weymouth D, Poliquin C, Vanderklish J, Sachs DH, Sykes M, Spitzer TR: Successful allogeneic stem cell transplantation with nonmyeloablative conditioning in patients with relapsed hematologic malignancy following autologous stem cell transplantation. Biol Blood Marrow Transplant; 2001;7(11):604-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Successful allogeneic stem cell transplantation with nonmyeloablative conditioning in patients with relapsed hematologic malignancy following autologous stem cell transplantation.
  • The use of myeloablative preparative therapy and allogeneic stem cell transplantation (alloSCT) as salvage therapy for adult patients with relapsed hematologic malignancy after autologous stem cell transplantation (autoSCT) is generally unsuccessful due to very high treatment-related mortality rates.
  • We evaluated the outcome of HLA-matched related donor alloSCT following nonmyeloablative preparative therapy in 13 patients (median age, 38 years) with relapsed hematologic malignancies (Hodgkin's disease, n = 4; Hodgkin's disease and advanced myelodysplastic syndrome, n = 1; non-Hodgkin's lymphoma, n = 6; multiple myeloma, n = 2) after initial autoSCT.
  • Median time from autoSCT to alloSCT was 12 months (range, 3-24 months); 6 patients had chemotherapy-refractory disease following autoSCT, 6 were in untreated relapse, and 1 had a partial response from salvage chemotherapy.
  • Preparative therapy consisted of cyclophosphamide, 150-200 mg/kg; peritransplantation anti-thymocyte globulin; thymic irradiation (in patients who had not received previous mediastinal irradiation); and a very short course of cyclosporine as GVHD prophylaxis.
  • The median survival time of the 13 patients is currently 10 months (range, 3-39 months), with an overall survival probability at 2 years of 45% (95% confidence interval [CI], 19%-73%) and a disease-free survival probability at 2 years of 37.5% (95% CI, 12%-65%).
  • Thus, this novel nonmyeloablative alloSCT strategy followed by prophylactic DLI was well tolerated and can result in durable disease-free survival among patients with advanced hematologic malignancies after a failed autoSCT.
  • Further follow-up and evaluation of additional patients are required to conclusively establish the role of this strategy in the treatment of hematologic malignancies after an autologous transplantation.
  • [MeSH-major] Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / methods. Immunosuppressive Agents / administration & dosage. Salvage Therapy / methods. Transplantation Conditioning / methods

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  • (PMID = 11760148.001).
  • [ISSN] 1083-8791
  • [Journal-full-title] Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation
  • [ISO-abbreviation] Biol. Blood Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 RO1 CA79986-O1A1; United States / NCI NIH HHS / CA / 1 RO1 CA79988-O1A1
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents
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4. Mone A, Puhalla S, Whitman S, Baiocchi RA, Cruz J, Vukosavljevic T, Banks A, Eisenbeis CF, Byrd JC, Caligiuri MA, Porcu P: Durable hematologic complete response and suppression of HTLV-1 viral load following alemtuzumab in zidovudine/IFN-{alpha}-refractory adult T-cell leukemia. Blood; 2005 Nov 15;106(10):3380-2
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  • [Title] Durable hematologic complete response and suppression of HTLV-1 viral load following alemtuzumab in zidovudine/IFN-{alpha}-refractory adult T-cell leukemia.
  • Adult T-cell leukemia (ATL) is a highly chemoresistant and usually fatal T-cell malignancy due to the human T-cell lymphotropic virus-1 (HTLV-1).
  • After chemotherapy failure, antiretrovirals and interferon-alpha (IFN-alpha) produce brief responses followed by progression and death.
  • A patient with refractory chronic ATL in transformation achieved longer than a 1-year complete hematologic response following 12 weeks of outpatient subcutaneous alemtuzumab.

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  • (PMID = 16076875.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / K23 CA10215-02; United States / NCI NIH HHS / CA / P01 CA95426; United States / NCI NIH HHS / CA / T32 CA009338
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 0 / Antigens, CD; 0 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / CD52 antigen; 0 / Glycoproteins; 0 / Interferon-alpha; 0 / Tumor Suppressor Protein p53; 3A189DH42V / alemtuzumab; 4B9XT59T7S / Zidovudine
  • [Other-IDs] NLM/ PMC1895052
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5. Spitzer TR, McAfee SL, Dey BR, Colby C, Hope J, Grossberg H, Preffer F, Shaffer J, Alexander SI, Sachs DH, Sykes M: Nonmyeloablative haploidentical stem-cell transplantation using anti-CD2 monoclonal antibody (MEDI-507)-based conditioning for refractory hematologic malignancies. Transplantation; 2003 May 27;75(10):1748-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nonmyeloablative haploidentical stem-cell transplantation using anti-CD2 monoclonal antibody (MEDI-507)-based conditioning for refractory hematologic malignancies.
  • Twelve patients (three cohorts of four patients each) received cyclophosphamide, MEDI-507, and haploidentical unmanipulated bone marrow (n=8) or ex vivo T-cell-depleted peripheral blood stem cells (n=4) for chemorefractory hematologic malignancy.
  • Nonmyeloablative preparative therapy with MEDI-507 and haploidentical SCT have led to the reliable induction of at least transient mixed chimerism as a potential platform for adoptive cellular immunotherapy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD2 / immunology. Hematologic Neoplasms / surgery. Stem Cell Transplantation. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Bone Marrow / physiology. Bone Marrow Transplantation. Cohort Studies. Cyclophosphamide / therapeutic use. Drug Administration Schedule. Graft Rejection / epidemiology. Haploidy. Humans. Immunosuppressive Agents / therapeutic use. Incidence. Middle Aged. Stem Cells / physiology. Transplantation Chimera

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  • (PMID = 12777868.001).
  • [ISSN] 0041-1337
  • [Journal-full-title] Transplantation
  • [ISO-abbreviation] Transplantation
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA79986-02; United States / NHLBI NIH HHS / HL / R01 HL63474
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD2; 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide
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6. McAfee SL, Powell SN, Colby C, Spitzer TR: Dose-escalated total body irradiation and autologous stem cell transplantation for refractory hematologic malignancy. Int J Radiat Oncol Biol Phys; 2002 May 1;53(1):151-6
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  • [Title] Dose-escalated total body irradiation and autologous stem cell transplantation for refractory hematologic malignancy.
  • PURPOSE: To evaluate the feasibility of dose escalation of total body irradiation (TBI) above the previously reported maximally tolerated dose, we have undertaken a Phase I-II trial of dose-escalated TBI with autologous peripheral blood stem cell transplantation (PBSCT) for chemotherapy-refractory lymphoma.
  • METHODS AND MATERIALS: Nine lymphoma patients with primary refractory disease (PRD) or in resistant relapse (RR) received dose-escalated TBI and PBSCT.
  • Interstitial pneumonitis developed in 1 patient who received 1,800 cGy after receiving recombinant alpha-interferon (with exacerbation after rechallenge with interferon).
  • CONCLUSION: TBI in a dose range 1,600-2,000 cGy as preparative therapy for autologous PBSCT is feasible and has substantial activity in chemorefractory non-Hodgkin's and Hodgkin's lymphoma.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation. Hodgkin Disease / therapy. Lymphoma, Non-Hodgkin / therapy. Whole-Body Irradiation / adverse effects
  • [MeSH-minor] Adult. Combined Modality Therapy. Dose Fractionation. Feasibility Studies. Female. Humans. Male. Middle Aged. Pilot Projects. Transplantation, Autologous

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  • (PMID = 12007954.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
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7. Gürman G, Arat M, Ilhan O, Konuk N, Beksaç M, Celebi H, Ozcan M, Arslan O, Ustün C, Akan H, Uysal A, Koç H: Allogeneic hematopoietic cell transplantation without myeloablative conditioning for patients with advanced hematologic malignancies. Cytotherapy; 2001;3(4):253-60
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  • [Title] Allogeneic hematopoietic cell transplantation without myeloablative conditioning for patients with advanced hematologic malignancies.
  • BACKGROUND: The effect of allogeneic hematopoietic cell transplantation (alloHCT) on hematologic malignancies is based on the graft-versus-malignancy effect.
  • Once mixed chimeric status, and host versus graft with graft versus host tolerance are achieved, further strengthening of chimerism and graft-versus-malignancy effect can be obtained by donor lymphocyte infusions (DLIs) when needed.
  • METHODS: The patient group consisted of 13 patients with advanced hematological malignancies: seven had CML, four of them in blastic-, two in chronic- and the remainder in accelerated-phase; four patients with AML, refractory or in second remission state; one patient with primary refractory secondary AML; and one patient with ALL relapsed after alloHCT.
  • Two CML patients in blastic phase (CML-BP), and the primary refractory secondary AML patient did not respond to procedure.
  • In four patients, drug therapy in conventional doses was added to post-transplant DLIs for their relapsed or refractory diseases.
  • A patient with CML-BP achieved CR and full donor chimerism after transplantation, but developed refractory post-transplant lymphoproliferative disease in the 19th month.
  • Two patients with refractory AML, one patient with relapsed ALL and two patients with CML in chronic phase were in complete chimeric status and free of disease signs.
  • Acute GvHD, Grade II-III, was observed in five patients, and two of them developed secondary progressive chronic GvHD subsequently.
  • We observed one early death in a platelet transfusion refractory blastic phase CML patient due to intracranial hemorrhage.
  • Procedure-related severe toxicity was not observed, either in standard-risk patients or stem-cell donors.
  • The second step, which was the result of the graft-versus-malignancy effect, could be seen in most of the patients, but was not sustained in all of them because of the aggressiveness of their malignancy.
  • The role of NMA conditioning, and of the treatment in standard disease indications, remains to be determined in further studies.
  • [MeSH-major] Graft Survival / immunology. Graft vs Tumor Effect / immunology. Hematologic Neoplasms / immunology. Hematologic Neoplasms / therapy. Hematopoietic Stem Cell Transplantation / methods. Hematopoietic Stem Cells / immunology. Immunosuppressive Agents / therapeutic use. Transplantation Conditioning / methods
  • [MeSH-minor] Adult. Bone Marrow Purging / adverse effects. Female. Graft vs Host Disease / immunology. Graft vs Host Disease / physiopathology. Host vs Graft Reaction / immunology. Humans. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / immunology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / physiopathology. Leukemia, Myelogenous, Chronic, BCR-ABL Positive / therapy. Leukemia, Myeloid, Acute / immunology. Leukemia, Myeloid, Acute / physiopathology. Leukemia, Myeloid, Acute / therapy. Male. Middle Aged. Myeloablative Agonists / therapeutic use. Postoperative Complications / etiology. Postoperative Complications / physiopathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / immunology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / physiopathology. Precursor Cell Lymphoblastic Leukemia-Lymphoma / therapy. Remission Induction / methods. Secondary Prevention. Transplantation Chimera / immunology. Transplantation, Homologous. Treatment Failure

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  • (PMID = 12171713.001).
  • [ISSN] 1465-3249
  • [Journal-full-title] Cytotherapy
  • [ISO-abbreviation] Cytotherapy
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 0 / Myeloablative Agonists
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8. Roecker AM, Stockert A, Kisor DF: Nelarabine in the treatment of refractory T-cell malignancies. Clin Med Insights Oncol; 2010 Dec 01;4:133-41
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  • [Title] Nelarabine in the treatment of refractory T-cell malignancies.
  • Nelarabine is a nucleoside analog indicated for the treatment of adult and pediatric patients with T-cell acute lymphoblastic leukemia (T-ALL) or T-cell lymphoblastic lymphoma (T-LBL) that is refractory or has relapsed after treatment with at least two chemotherapy regimens.
  • After being first synthesized in the late 1970s and receiving FDA approval in 2005, the appropriate use of nelarabine for refractory hematologic malignancies is still being elucidated.
  • Dose-dependent toxicities, including neurotoxicity and myelosuppression, have been documented and may, in turn, limit the ability to appropriately treat the diagnosed malignancy.
  • This article will summarize the pharmacologic properties of nelarabine and will address the current place in therapy nelarabine holds based upon the results of the available clinical trials to date.

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  • (PMID = 21151585.001).
  • [ISSN] 1179-5549
  • [Journal-full-title] Clinical Medicine Insights. Oncology
  • [ISO-abbreviation] Clin Med Insights Oncol
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2999959
  • [Keywords] NOTNLM ; Arranon / Atriance / T-cell / leukemia / lymphoma / nelarabine
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9. Raad II, Hachem RY, Herbrecht R, Graybill JR, Hare R, Corcoran G, Kontoyiannis DP: Posaconazole as salvage treatment for invasive fusariosis in patients with underlying hematologic malignancy and other conditions. Clin Infect Dis; 2006 May 15;42(10):1398-403
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  • [Title] Posaconazole as salvage treatment for invasive fusariosis in patients with underlying hematologic malignancy and other conditions.
  • BACKGROUND: Conventional amphotericin B-based antifungal therapy for invasive fusariosis in patients with a hematologic malignancy results in a > or = 70% failure rate.
  • METHODS: In this retrospective analysis of patients from 3 open-label clinical trials, we evaluated posaconazole for the treatment of invasive fusariosis.
  • Twenty-one patients with proven or probable invasive fusariosis who had disease refractory to or who were intolerant of standard antifungal therapy received oral posaconazole suspension (800 mg per day in divided doses) as salvage therapy.
  • Among patients with leukemia who received posaconazole therapy for >3 days, the overall success rate was 50%; for patients who recovered from myelosuppression, the success rate was 67%, compared with 20% for those with persistent neutropenia.
  • CONCLUSION: These results suggest that posaconazole is useful for the treatment of invasive fusariosis.
  • [MeSH-major] Antifungal Agents / therapeutic use. Fusarium. Leukemia / complications. Mycoses / drug therapy. Salvage Therapy. Triazoles / therapeutic use
  • [MeSH-minor] Adult. Aged. Amphotericin B / therapeutic use. Female. Humans. Male. Middle Aged. Retrospective Studies. Treatment Outcome


10. Kaufman J, Gleason C, Lonial S: Treatment of relapsed and refractory myeloma. Curr Hematol Malig Rep; 2009 Apr;4(2):99-107
Hazardous Substances Data Bank. THALIDOMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of relapsed and refractory myeloma.
  • Treatment options for patients with relapsed and refractory myeloma have dramatically changed as a result of the approval of bortezomib, thalidomide, lenalidomide, and bortezomib/liposomal doxorubicin by the US Food and Drug Administration.
  • These changes have resulted in improved responses to salvage therapy and, in many cases, improved overall survival.
  • The challenge for clinicians is choosing which agent to use and deciding whether a single agent or combination therapy is the optimal treatment option for each patient.
  • This article outlines some of the data underpinning the use of bortezomib, thalidomide, lenalidomide, or combinations of these agents in the setting of relapsed myeloma, as well as a number of potential future agents or combinations that may improve outcomes for patients with relapsed and refractory disease.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Multiple Myeloma / drug therapy
  • [MeSH-minor] Antineoplastic Agents / administration & dosage. Antineoplastic Agents / therapeutic use. Boronic Acids / administration & dosage. Boronic Acids / therapeutic use. Bortezomib. Dexamethasone / administration & dosage. Dexamethasone / therapeutic use. Drug Resistance, Neoplasm. Humans. Neoplasm Recurrence, Local. Pyrazines / administration & dosage. Pyrazines / therapeutic use. Thalidomide / administration & dosage. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use

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  • (PMID = 20425421.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 4Z8R6ORS6L / Thalidomide; 69G8BD63PP / Bortezomib; 7S5I7G3JQL / Dexamethasone; F0P408N6V4 / lenalidomide
  • [Number-of-references] 77
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11. Tsukune Y, Isobe Y, Yasuda H, Shimizu S, Katsuoka Y, Hosone M, Oshimi K, Komatsu N, Sugimoto K: Activity and safety of combination chemotherapy with methotrexate, ifosfamide, l-asparaginase and dexamethasone (MILD) for refractory lymphoid malignancies: a pilot study. Eur J Haematol; 2010 Apr;84(4):310-5
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activity and safety of combination chemotherapy with methotrexate, ifosfamide, l-asparaginase and dexamethasone (MILD) for refractory lymphoid malignancies: a pilot study.
  • Optimal salvage chemotherapy has not been established for lymphoid malignancy, which is refractory to the conventional cyclophosphamide, doxorubicin, vincristine, and prednisone regimen.
  • To explore an effective regimen, we conducted a phase I pilot study of combination chemotherapy with methotrexate, ifosfamide, l-asparaginase and dexamethasone (MILD), which are unaffected by MDR1-encoded P-glycoprotein.
  • A total of 18 patients with lethal lymphoid malignancy were enrolled over a 2-yr period.
  • Eleven patients completed two courses of MILD therapy.
  • Treatment-related death because of systemic mucormycosis was observed in one patient.
  • Major treatment-related adverse events were grade 3 or more hematologic toxicities, which included lymphopenia corresponding to dose-limiting toxicity.
  • The most common grade 3 non-hematologic toxicity was febrile neutropenia.
  • MILD therapy was feasible and presented acceptable toxicity in patients with refractory or lethal lymphoid malignancies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Hematologic Neoplasms / drug therapy

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  • (PMID = 20015242.001).
  • [ISSN] 1600-0609
  • [Journal-full-title] European journal of haematology
  • [ISO-abbreviation] Eur. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] EC 3.5.1.1 / Asparaginase; UM20QQM95Y / Ifosfamide; YL5FZ2Y5U1 / Methotrexate
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12. Ludwig H, Khayat D, Giaccone G, Facon T: Proteasome inhibition and its clinical prospects in the treatment of hematologic and solid malignancies. Cancer; 2005 Nov 1;104(9):1794-807
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proteasome inhibition and its clinical prospects in the treatment of hematologic and solid malignancies.
  • Preclinical studies have shown that the proteasome inhibitor bortezomib decreases proliferation, induces apoptosis, enhances the activity of chemotherapy and radiation, and reverses chemoresistance in a variety of hematologic and solid malignancy models in vitro and in vivo.
  • In two Phase II trials, SUMMIT and CREST, it was found that treatment with bortezomib, alone or in combination with dexamethasone, produced durable responses with meaningful survival benefits in patients with recurrent and/or refractory multiple myeloma.
  • Clinical trials evaluating the safety and activity of bortezomib alone or in combination regimens with dexamethasone, doxorubicin, melphalan, prednisone, and/or thalidomide in the treatment of patients with newly diagnosed multiple myeloma have shown encouraging results.
  • Preliminary studies suggest that bortezomib may serve as induction therapy before stem cell transplantation.
  • Further studies with bortezomib as monotherapy and in combination regimens in the treatment of solid and hematologic malignancies are warranted.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Hematologic Neoplasms / drug therapy. Neoplasms / drug therapy. Proteasome Inhibitors. Pyrazines / therapeutic use
  • [MeSH-minor] Apoptosis. Bortezomib. Clinical Trials as Topic. Humans. Models, Molecular. Multiple Myeloma / drug therapy. Protease Inhibitors / adverse effects. Protease Inhibitors / therapeutic use. Proteasome Endopeptidase Complex / chemistry. Proteasome Endopeptidase Complex / physiology. Tumor Cells, Cultured

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  • [Copyright] (c) 2005 American Cancer Society.
  • (PMID = 16178003.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Number-of-references] 79
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13. Wakabayashi S, Ohashi K: [Oral molecular targeting agents in hematological malignancy]. Gan To Kagaku Ryoho; 2010 Jul;37(7):1214-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Oral molecular targeting agents in hematological malignancy].
  • Molecular target therapy is progressive and promising in various hematological malignancies.
  • Imatinib is now the treatment of choice for chronic-phase chronic myeloid leukemia.
  • Eight-year data from the pivotal trial of imatinib, the IRIS trial, showed high long-term response rates and favorable tolerability profile compared with previous therapies.
  • For patients with primary resistance to imatinib, hematologic disease recurrence, or emergent BCR-ABL kinase domain mutations, the potent second generation tyrosine kinase inhibitors dasatinib and nilotinib are now available.
  • Since the introduction of all-trans retinoic acid (ATRA) in the 1980s, the strategy for treating acute promyelocytic leukemia (APL) has shifted from conventional chemotherapy to cell differentiation.
  • The combination of ATRA and anthracycline-based chemotherapy is currently the standard approach to treat newly-diagnosed APL.
  • Multiple myeloma (MM) is also one of the major therapeutic targets in using molecular based technology.
  • The recent availability of clinical data regarding thalidomide and lenalidomide has provided effective treatment options for patients with both newly diagnosed and relapsed/refractory MM.
  • Overall, this paper focuses on a comprehensive review of the current literature and provides data supporting molecular target therapy for patients with CML, APL, or MM.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematologic Neoplasms / drug therapy. Hematologic Neoplasms / metabolism

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  • (PMID = 20647701.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 14
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14. Osterborg A, Karlsson C, Lundin J: Alemtuzumab to treat refractory autoimmune hemolytic anemia or thrombocytopenia in chronic lymphocytic leukemia. Curr Hematol Malig Rep; 2009 Jan;4(1):47-53
Hazardous Substances Data Bank. PREDNISONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alemtuzumab to treat refractory autoimmune hemolytic anemia or thrombocytopenia in chronic lymphocytic leukemia.
  • Conventional therapies for these autoimmune disorders, such as corticosteroids, splenectomy, and immunosuppressive agents, may not induce complete resolution in all patients, and relapses are common.
  • In recent years, monoclonal antibodies such as alemtuzumab and rituximab, already used successfully for the management of lymphoproliferative disorders, have been shown to be effective in the treatment of a range of autoimmune disorders.
  • Results from a range of reports confirm the efficacy of alemtuzumab for the treatment of severe, CLL-related autoimmune cytopenias that have failed to respond to conventional therapies and may even be rituximab-refractory.
  • [MeSH-major] Anemia, Hemolytic, Autoimmune / drug therapy. Antibodies, Monoclonal / therapeutic use. Antibodies, Neoplasm / therapeutic use. Antineoplastic Agents / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Thrombocytopenia / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Clinical Trials as Topic. Humans. Immunosuppressive Agents / therapeutic use. Prednisone / therapeutic use. Rituximab

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  • (PMID = 20425438.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / Immunosuppressive Agents; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab; VB0R961HZT / Prednisone
  • [Number-of-references] 39
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15. O'Connor OA, Heaney ML, Schwartz L, Richardson S, Willim R, MacGregor-Cortelli B, Curly T, Moskowitz C, Portlock C, Horwitz S, Zelenetz AD, Frankel S, Richon V, Marks P, Kelly WK: Clinical experience with intravenous and oral formulations of the novel histone deacetylase inhibitor suberoylanilide hydroxamic acid in patients with advanced hematologic malignancies. J Clin Oncol; 2006 Jan 1;24(1):166-73
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical experience with intravenous and oral formulations of the novel histone deacetylase inhibitor suberoylanilide hydroxamic acid in patients with advanced hematologic malignancies.
  • PURPOSE: To document the toxicity and activity of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) in patients with pretreated hematologic malignancies.
  • In both trials, dose escalation was performed in parallel and independently in patients with solid tumors and hematologic malignancies.
  • RESULTS: A total of 39 patients with hematologic malignancy were enrolled (14 on IV SAHA and 25 on oral SAHA), of whom 35 were treated.
  • Typically, the hematologic toxicities resolved shortly after SAHA was stopped.
  • One patient with refractory HD had a PR, whereas three patients had stable disease for up to 9 months.
  • CONCLUSION: These results suggest that SAHA has activity in hematologic malignancies including HD and select subtypes of non-Hodgkin's lymphoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Enzyme Inhibitors / therapeutic use. Hematologic Neoplasms / drug therapy. Histone Deacetylase Inhibitors. Hydroxamic Acids / administration & dosage


16. Kennedy B, Rawstron A, Carter C, Ryan M, Speed K, Lucas G, Hillmen P: Campath-1H and fludarabine in combination are highly active in refractory chronic lymphocytic leukemia. Blood; 2002 Mar 15;99(6):2245-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Campath-1H and fludarabine in combination are highly active in refractory chronic lymphocytic leukemia.
  • Combination therapy is now the conventional treatment for most hematologic malignancies.
  • Monoclonal antibody treatments may sensitize tumor cells to subsequent chemotherapy.
  • We report the combination of Campath-1H with fludarabine in patients with CLL refractory to each agent used singly.
  • Five patients responded, including one who had a complete response by National Cancer Institute criteria.
  • Campath-1H combined with fludarabine is a highly promising novel therapy for refractory CLL.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antibodies, Neoplasm / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy. Vidarabine / administration & dosage
  • [MeSH-minor] Adult. Aged. Antibodies, Monoclonal, Humanized. Bone Marrow / pathology. Drug Resistance. Humans. Male. Middle Aged. Remission Induction. Therapeutic Equivalency. Treatment Outcome

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  • (PMID = 11877305.001).
  • [ISSN] 0006-4971
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Neoplasm; 3A189DH42V / alemtuzumab; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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17. Chung HJ, Seo EJ, Kim KH, Jang S, Park CJ, Chi HS, Lee JH, Lee JH, Lee KH: [Hematologic and clinical features of 3q21q26 syndrome: extremely poor prognosis and association with central diabetes insipidus]. Korean J Lab Med; 2007 Apr;27(2):133-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Hematologic and clinical features of 3q21q26 syndrome: extremely poor prognosis and association with central diabetes insipidus].
  • METHODS: From May 2001 to June 2006, a total of 5 patients with hematologic malignancy were found to have 3q21q26 syndrome and monosomy 7.
  • RESULTS: The rearrangement type of 3q21q26 was inv(3)(q21q26) in four patients and t(3;3)(q21;. q26) in one.
  • These patients' French American British types were AML M1, M2, M4 and M7, showing evident dysmegakaryopoiesis.
  • All the five patients were refractory or in early relapse.
  • While DI was well controlled with oral desmopressin, leukemia was refractory to chemotherapy.
  • [MeSH-major] Chromosome Disorders / complications. Chromosome Disorders / diagnosis. Chromosomes, Human, Pair 3. Diabetes Insipidus, Neurogenic / complications. Hematologic Neoplasms / complications

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  • (PMID = 18094565.001).
  • [ISSN] 1598-6535
  • [Journal-full-title] The Korean journal of laboratory medicine
  • [ISO-abbreviation] Korean J Lab Med
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Korea (South)
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18. Picardi A, Fabritiis Pd Pd, Cudillo L, Dentamaro T, Cupelli L, Ballatore G, Venditti A, Caravita T, Cristina Cox M, Catalano G, Amadori S: Possibility of long-term remission in patients with advanced hematologic malignancies after reduced intensity conditioning regimen (RIC) and allogeneic stem cell transplantation. Hematol J; 2004;5(1):24-31
Hazardous Substances Data Bank. CYCLOSPORIN A .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Possibility of long-term remission in patients with advanced hematologic malignancies after reduced intensity conditioning regimen (RIC) and allogeneic stem cell transplantation.
  • High-dose chemotherapy and radiation used as a preparative regimen for allogeneic stem cell transplantation (SCT) produces a considerable morbidity and mortality.
  • An alternative strategy, developed to reduce transplant-related toxicity and to induce graft versus malignancy effect in the presence of full hematopoietic engraftment, includes the application of RIC that provide sufficient immunosuppression.
  • In all, 22 patients with hematologic malignancies and HLA-identical sibling donors were included in this study.
  • All patients were either refractory to therapy or beyond first complete remission (CR).
  • All the durable responses occurred in patients who developed GVHD.
  • provide durable responses in patients not eligible for conventional SCT exploiting the graft-versus-malignancy effect and (3).

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  • (PMID = 14745426.001).
  • [ISSN] 1466-4860
  • [Journal-full-title] The hematology journal : the official journal of the European Haematology Association
  • [ISO-abbreviation] Hematol. J.
  • [Language] ENG
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 83HN0GTJ6D / Cyclosporine; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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19. Morgan-Meadows S, Thomas JP, Mulkerin D, Berlin JD, Bailey H, Binger K, Volkman J, Alberti D, Feierabend C, Marrocha R, Arzoomanian RZ, Wilding G: Phase I study of eniluracil, oral 5-fluororacil and gemcitabine in patients with advanced malignancy. Invest New Drugs; 2002 Nov;20(4):377-82
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase I study of eniluracil, oral 5-fluororacil and gemcitabine in patients with advanced malignancy.
  • PATIENTS AND METHODS: Patients with histologically confirmed, incurable malignancy (solid tumor or lymphoma) refractory to standard therapy or for which no standard therapy exists were enrolled.
  • The treatment plan consisted of weekly gemcitabine for three weeks with twice daily dosing of 5-FU and eniluracil for 21 days beginning on day one of gemcitabine.
  • Eight patients received less than 2 cycles of therapy.
  • Hematologic and gastrointestinal toxicity predominated, with 48% of courses resulted in grade one or two neutropenia.
  • Hematologic toxicity was dose limiting.
  • One treatment related death occurred.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Fluorouracil / administration & dosage. Lymphoma / drug therapy. Uracil / administration & dosage. Uracil / analogs & derivatives
  • [MeSH-minor] Administration, Oral. Female. Humans. Male. Middle Aged. Neoplasms / drug therapy. Patients / statistics & numerical data

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  • (PMID = 12448654.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0W860991D6 / Deoxycytidine; 2E2W0W5XIU / eniluracil; 56HH86ZVCT / Uracil; B76N6SBZ8R / gemcitabine; U3P01618RT / Fluorouracil
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20. Schmidt-Hieber M, Fietz T, Knauf W, Uharek L, Hopfenmüller W, Thiel E, Blau IW: Efficacy of the interleukin-2 receptor antagonist basiliximab in steroid-refractory acute graft-versus-host disease. Br J Haematol; 2005 Aug;130(4):568-74
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Efficacy of the interleukin-2 receptor antagonist basiliximab in steroid-refractory acute graft-versus-host disease.
  • We conducted a prospective phase II trial to assess the efficacy and feasibility of treating steroid-refractory aGVHD with basiliximab, a chimaeric monoclonal antibody directed against the alpha chain of the interleukin-2 (IL-2) receptor.
  • The rates of infections, chronic GVHD, malignancy recurrence and 1-year TRM following immunosuppression with basiliximab were comparable with those found with other treatment modalities for aGVHD.
  • We conclude that basiliximab is efficient and feasible for steroid-refractory aGVHD and merits further evaluation.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Graft vs Host Disease / drug therapy. Hematopoietic Stem Cell Transplantation. Immunosuppressive Agents / therapeutic use. Receptors, Interleukin-2 / antagonists & inhibitors. Recombinant Fusion Proteins / therapeutic use
  • [MeSH-minor] Acute Disease. Adult. Drug Tolerance. Feasibility Studies. Female. Follow-Up Studies. Hematologic Neoplasms / surgery. Humans. Male. Middle Aged. Prospective Studies. Steroids / therapeutic use. Transplantation Conditioning. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 16098072.001).
  • [ISSN] 0007-1048
  • [Journal-full-title] British journal of haematology
  • [ISO-abbreviation] Br. J. Haematol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Immunosuppressive Agents; 0 / Receptors, Interleukin-2; 0 / Recombinant Fusion Proteins; 0 / Steroids; 0 / basiliximab
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21. Maertens J, Raad I, Petrikkos G, Boogaerts M, Selleslag D, Petersen FB, Sable CA, Kartsonis NA, Ngai A, Taylor A, Patterson TF, Denning DW, Walsh TJ, Caspofungin Salvage Aspergillosis Study Group: Efficacy and safety of caspofungin for treatment of invasive aspergillosis in patients refractory to or intolerant of conventional antifungal therapy. Clin Infect Dis; 2004 Dec 1;39(11):1563-71
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  • [Title] Efficacy and safety of caspofungin for treatment of invasive aspergillosis in patients refractory to or intolerant of conventional antifungal therapy.
  • METHODS: We investigated the efficacy and safety of caspofungin in the treatment of IA.
  • Ninety patients with IA who were refractory to or intolerant of amphotericin B, lipid formulations of amphotericin B, or triazoles were enrolled to receive caspofungin.
  • RESULTS: Efficacy was assessed for 83 patients who had infection consistent with definitions of IA and who received >or=1 dose of study drug.
  • Common underlying conditions included hematologic malignancy (48% of patients), allogeneic blood and marrow transplantation (25% of patients), and solid-organ transplantation (11% of patients).
  • Seventy-one patients (86%) were refractory to and 12 patients (14%) were intolerant of previous therapy.
  • A favorable response to caspofungin therapy was observed in 37 (45%) of 83 patients, including 32 (50%) of 64 with pulmonary aspergillosis and 3 (23%) of 13 with disseminated aspergillosis.
  • Two patients discontinued caspofungin therapy because of drug-related adverse events.
  • Drug-related nephrotoxicity and hepatotoxicity occurred infrequently.
  • CONCLUSION: Caspofungin demonstrated usefulness in the salvage treatment of IA.
  • [MeSH-major] Antifungal Agents / therapeutic use. Aspergillosis / drug therapy. Peptides, Cyclic / therapeutic use
  • [MeSH-minor] Adolescent. Aged. Echinocandins. Female. Humans. Male. Middle Aged. Treatment Failure

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  • (PMID = 15578352.001).
  • [ISSN] 1537-6591
  • [Journal-full-title] Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
  • [ISO-abbreviation] Clin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antifungal Agents; 0 / Echinocandins; 0 / Peptides, Cyclic; F0XDI6ZL63 / caspofungin
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22. McNall-Knapp RY, Williams CN, Reeves EN, Heideman RL, Meyer WH: Extended phase I evaluation of vincristine, irinotecan, temozolomide, and antibiotic in children with refractory solid tumors. Pediatr Blood Cancer; 2010 Jul 1;54(7):909-15
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extended phase I evaluation of vincristine, irinotecan, temozolomide, and antibiotic in children with refractory solid tumors.
  • PROCEDURE: Patients under 22 years with recurrent or refractory solid tumors were eligible.
  • A course of chemotherapy was given every 28 days.
  • Hematologic toxicity was mild and not prolonged.
  • CONCLUSIONS: This combination is safe and shows activity in pediatric patients with recurrent malignancy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neoplasms / drug therapy

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  • [Copyright] Copyright 2010 Wiley-Liss, Inc.
  • (PMID = 20405511.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase I; Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 5J49Q6B70F / Vincristine; 7673326042 / irinotecan; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; XT3Z54Z28A / Camptothecin
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23. White CA, Weaver RL, Grillo-López AJ: Antibody-targeted immunotherapy for treatment of malignancy. Annu Rev Med; 2001;52:125-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antibody-targeted immunotherapy for treatment of malignancy.
  • Despite testing since the mid-1900s, only in the past three years have some monoclonal antibodies provided sufficient efficacy and safety data to support regulatory approval as cancer therapy.
  • Adjuvant-edrecolomab monoclonal antibody was approved in Germany after demonstration of a statistically significant 32% improvement over observation alone in the seven-year mortality rate for patients with colorectal cancer.
  • Similarly, trastuzumab monoclonal antibody combined with chemotherapy prolonged the median time to the progression of breast cancer compared to chemotherapy alone.
  • Unconjugated monoclonal antibodies investigated for the treatment of hematologic malignancies include anti-idiotype, CAMPATH-1, and rituximab.
  • Rituximab was the first such therapy approved in the United States for relapsed or refractory low-grade or follicular B-cell non-Hodgkin's lymphoma after demonstration of an overall response rate of 48% and a duration of response of 11.7 months.
  • The radioisotope-conjugated monoclonal antibodies tested as therapy include anti-B1, LYM-1, LL2, anti-CD33, and ibritumomab tiuxetan.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Immunotherapy / methods. Neoplasms / therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Combined Modality Therapy. Disease Progression. Humans. Rituximab. Trastuzumab. Treatment Outcome

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  • [ErratumIn] Annu Rev Med 2002;53:xi
  • (PMID = 11160771.001).
  • [ISSN] 0066-4219
  • [Journal-full-title] Annual review of medicine
  • [ISO-abbreviation] Annu. Rev. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antineoplastic Agents; 0 / Edrecolomab; 4F4X42SYQ6 / Rituximab; P188ANX8CK / Trastuzumab
  • [Number-of-references] 108
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24. Coiffier B, Ribrag V: Exploring mammalian target of rapamycin (mTOR) inhibition for treatment of mantle cell lymphoma and other hematologic malignancies. Leuk Lymphoma; 2009 Dec;50(12):1916-30
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  • [Title] Exploring mammalian target of rapamycin (mTOR) inhibition for treatment of mantle cell lymphoma and other hematologic malignancies.
  • The mammalian target of rapamycin (mTOR) pathway regulates translation of key proteins that contribute to the pathogenesis of advanced hematologic malignancies.
  • Inhibitors of mTOR (temsirolimus, everolimus, and deforolimus) constitute a new class of antitumor agents, with potential for treatment of relapsed and/or refractory hematologic malignancies.
  • Mantle cell lymphoma (MCL) was the first hematologic malignancy in which mTOR inhibition was explored as a treatment strategy, owing to its characteristic overexpression of cyclin D1, a G1 cyclin regulated by mTOR signaling.
  • Temsirolimus and everolimus exhibited antitumor activity against relapsed, refractory disease in phase II studies.
  • In a randomized phase III trial, once-weekly intravenous temsirolimus 175 mg for 3 weeks followed by 75 mg once weekly was recently shown to improve progression-free survival (p=0.0009) and objective response rate (p=0.0019) versus investigator's choice of therapy in relapsed or refractory MCL.
  • Overall, the clinical findings to date strengthen mTOR inhibition as a novel and promising strategy for the treatment of certain hematologic malignancies, particularly for MCL.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Hematologic Neoplasms / drug therapy. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Lymphoma, Mantle-Cell / drug therapy. Protein-Serine-Threonine Kinases / antagonists & inhibitors
  • [MeSH-minor] Cyclin D1 / metabolism. Everolimus. Humans. Models, Biological. Sirolimus / analogs & derivatives. Sirolimus / therapeutic use. TOR Serine-Threonine Kinases

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  • (PMID = 19757306.001).
  • [ISSN] 1029-2403
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Intracellular Signaling Peptides and Proteins; 136601-57-5 / Cyclin D1; 48Z35KB15K / ridaforolimus; 624KN6GM2T / temsirolimus; 9HW64Q8G6G / Everolimus; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; W36ZG6FT64 / Sirolimus
  • [Number-of-references] 85
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25. Klein CE, Tangen CM, Braun TJ, Hussain MH, Peereboom DM, Nichols CR, Rivkin SE, Dakhil SR, Crawford ED: SWOG-9510: evaluation of topotecan in hormone refractory prostate cancer: a Southwest Oncology Group study. Prostate; 2002 Sep 1;52(4):264-8
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  • [Title] SWOG-9510: evaluation of topotecan in hormone refractory prostate cancer: a Southwest Oncology Group study.
  • BACKGROUND: Prostate cancer is the most common malignancy in American men, and as many as 70% of those initially treated for localized disease will ultimately progress and be considered candidates to receive therapy for metastatic cancer [Fuks et al.: Int J Radiat Oncol Bio Phys 21:537-547, 1991; Chodak et al.: N Engl J Med 330:246-248, 1994].
  • Although most will respond initially to hormone manipulation, essentially all will fail and require additional therapy.
  • No standard chemotherapy approach has been shown to prolong survival significantly, and new agents are desperately needed.
  • Topotecan is a new topoisomerase-1 inhibitor whose early investigation suggested possible activity in hormone-refractory prostate cancer.
  • METHODS: In this phase II trial, patients having failed one or two prior androgen ablative therapies were treated with 21-day continuous intravenous infusions of topotecan at a dose of 0.5 mg/m(2) per day every 28 days.
  • The most common toxicities were hematologic, with 8 of 24 assessable patients experiencing grade 4 toxicity.
  • CONCLUSION: Topotecan infusions at this dose are ineffective in the management of hormone-refractory prostate cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Prostatic Neoplasms / drug therapy. Topotecan / pharmacology
  • [MeSH-minor] Aged. Aged, 80 and over. Drug Resistance, Neoplasm. Humans. Infusions, Intravenous. Male. Middle Aged. Survival Analysis. Treatment Outcome

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12210486.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA04919; United States / NCI NIH HHS / CA / CA12213; United States / NCI NIH HHS / CA / CA14028; United States / NCI NIH HHS / CA / CA20319; United States / NCI NIH HHS / CA / CA32102; United States / NCI NIH HHS / CA / CA35281; United States / NCI NIH HHS / CA / CA35431; United States / NCI NIH HHS / CA / CA37981; United States / NCI NIH HHS / CA / CA38296; United States / NCI NIH HHS / CA / CA45560; United States / NCI NIH HHS / CA / CA45807; United States / NCI NIH HHS / CA / CA46113; United States / NCI NIH HHS / CA / CA58861; United States / NCI NIH HHS / CA / CA63844; United States / NCI NIH HHS / CA / CA76462; United States / NCI NIH HHS / CA / CA96429
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 7M7YKX2N15 / Topotecan
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26. Crawford LJ, Walker B, Irvine AE: Proteasome inhibitors: a therapeutic strategy for haematological malignancy. Front Biosci; 2008;13:4285-96
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  • [Title] Proteasome inhibitors: a therapeutic strategy for haematological malignancy.
  • In recent years, inhibition of proteasome function has emerged as a novel anti-cancer therapy.
  • Proteasome inhibition is now established as an effective treatment for relapsed and refractory multiple myeloma and offers great promise for the treatment of other haematological malignancies, when used in combination with conventional therapeutic agents.
  • Bortezomib is the first proteasome inhibitor to be used clinically and a second generation of proteasome inhibitors with differential pharmacological properties are currently in early clinical trials.
  • This review summarises the development of proteasome inhibitors as therapeutic agents and describes how novel assays for measuring proteasome activity and inhibition may help to further delineate the mechanisms of action of different proteasome inhibitors.
  • This will allow for the optimized use of proteasome inhibitors in combination therapies and provide the opportunity to design more potent and therapeutically efficacious proteasome inhibitors.
  • [MeSH-major] Hematologic Neoplasms / drug therapy. Protease Inhibitors / therapeutic use. Proteasome Inhibitors
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Bortezomib. Cell Nucleus / enzymology. Cytoplasm / enzymology. Humans. Leukemia / drug therapy. Proteasome Endopeptidase Complex. Pyrazines / therapeutic use. Ubiquitin / antagonists & inhibitors. Ubiquitin / metabolism

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  • (PMID = 18508511.001).
  • [ISSN] 1093-9946
  • [Journal-full-title] Frontiers in bioscience : a journal and virtual library
  • [ISO-abbreviation] Front. Biosci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 0 / Ubiquitin; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex; EC 3.4.99.- / ATP dependent 26S protease
  • [Number-of-references] 77
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27. Thomas X: The role of timed sequential chemotherapy in adult acute myelogenous leukemia. Curr Hematol Malig Rep; 2008 Apr;3(2):89-95
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  • [Title] The role of timed sequential chemotherapy in adult acute myelogenous leukemia.
  • Consecutive trials of timed sequential chemotherapy (TSC) have been conducted in adults with acute myelogenous leukemia.
  • The rationale for TSC was based on the observation that leukemic cells can be recruited synchronously into the cell cycle after initial intensive therapy, at which time they may become more susceptible to killing by chemotherapeutic agents.
  • This article reviews the results of important trials in which TSC was used as an induction regimen in de novo, relapsed, or refractory acute myelogenous leukemia or as postremission therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Leukemia, Myeloid, Acute / drug therapy
  • [MeSH-minor] Adult. Cell Cycle / drug effects. Clinical Trials as Topic. Drug Administration Schedule. Humans

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  • (PMID = 20425452.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 50
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28. Jackson G, Einsele H, Moreau P, Miguel JS: Bortezomib, a novel proteasome inhibitor, in the treatment of hematologic malignancies. Cancer Treat Rev; 2005 Dec;31(8):591-602
Hazardous Substances Data Bank. BORTEZOMIB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bortezomib, a novel proteasome inhibitor, in the treatment of hematologic malignancies.
  • Proteasome inhibition is a novel approach to treating malignancy, and bortezomib is the first proteasome inhibitor in this class to be approved for clinical use.
  • In preclinical studies, bortezomib caused cell cycle arrest and apoptosis in myeloma and lymphoma cell lines as well as in other neoplastic cell types.
  • Cyclical thrombocytopenia and peripheral neuropathy, which generally abate after cessation of treatment, are the most clinically significant toxicities.
  • Two phase II trials, SUMMIT and CREST, demonstrated impressive activity with bortezomib 1.3 mg/m2 monotherapy in relapsed and refractory myeloma, with an impressive 35% response rate (complete+partial+minimal responses) in SUMMIT and a 50% response rate in CREST, using the rigorous European Group for Blood and Marrow Transplantation criteria.
  • Results of ongoing trials with bortezomib in the first-line treatment of myeloma have been extremely encouraging and have demonstrated the benefit of using bortezomib as part of an induction regimen prior to stem cell transplantation.
  • Importantly, two clinical trials with bortezomib as monotherapy in refractory non-Hodgkin's lymphoma have shown impressive response rates, particularly in aggressive mantle cell lymphoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Hematologic Neoplasms / drug therapy. Pyrazines / therapeutic use
  • [MeSH-minor] Apoptosis / drug effects. Bortezomib. Cell Cycle / drug effects. Clinical Trials as Topic. Humans. Treatment Outcome

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  • (PMID = 16298074.001).
  • [ISSN] 0305-7372
  • [Journal-full-title] Cancer treatment reviews
  • [ISO-abbreviation] Cancer Treat. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 70
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29. O'Connor OA, Horwitz S, Hamlin P, Portlock C, Moskowitz CH, Sarasohn D, Neylon E, Mastrella J, Hamelers R, Macgregor-Cortelli B, Patterson M, Seshan VE, Sirotnak F, Fleisher M, Mould DR, Saunders M, Zelenetz AD: Phase II-I-II study of two different doses and schedules of pralatrexate, a high-affinity substrate for the reduced folate carrier, in patients with relapsed or refractory lymphoma reveals marked activity in T-cell malignancies. J Clin Oncol; 2009 Sep 10;27(26):4357-64
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Phase II-I-II study of two different doses and schedules of pralatrexate, a high-affinity substrate for the reduced folate carrier, in patients with relapsed or refractory lymphoma reveals marked activity in T-cell malignancies.
  • Patients were required to have relapsed/refractory disease, an absolute neutrophil greater than 1,000/microL, and a platelet count greater than 50,000/microL for the first dose of any cycle.
  • RESULTS: The every-other-week, phase II experience was associated with an increased risk of stomatitis and hematologic toxicity.
  • This schedule modification resulted in a 50% reduction in the major hematologic toxicities and abrogation of the grades 3 to 4 stomatitis.
  • All eight patients who experienced CR had T-cell lymphoma, and four of the six patients with a partial remission were positron emission tomography negative.
  • CONCLUSION: Pralatrexate has significant single-agent activity in patients with relapsed/refractory T-cell lymphoma.
  • [MeSH-major] Aminopterin / analogs & derivatives. Lymphoma, T-Cell / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Constipation / chemically induced. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Resistance, Neoplasm. Fatigue / chemically induced. Female. Folic Acid Antagonists / administration & dosage. Folic Acid Antagonists / adverse effects. Folic Acid Antagonists / therapeutic use. Humans. Male. Middle Aged. Recurrence. Remission Induction. Stomatitis / chemically induced. Treatment Outcome. Weight Loss / drug effects. Young Adult

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  • (PMID = 19652067.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Databank-accession-numbers] ClinicalTrials.gov/ NCT00052442
  • [Publication-type] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 10-propargyl-10-deazaaminopterin; 0 / Folic Acid Antagonists; JYB41CTM2Q / Aminopterin
  • [Other-IDs] NLM/ PMC3651599
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30. Dorr RT, Briggs A, Kintzel P, Meyers R, Chow HH, List A: Comparative pharmacokinetic study of high-dose etoposide and etoposide phosphate in patients with lymphoid malignancy receiving autologous stem cell transplantation. Bone Marrow Transplant; 2003 Apr;31(8):643-9
Hazardous Substances Data Bank. ETOPOSIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparative pharmacokinetic study of high-dose etoposide and etoposide phosphate in patients with lymphoid malignancy receiving autologous stem cell transplantation.
  • The pharmacokinetics of two etoposide (E) formulations were evaluated in patients with refractory hematologic malignancies receiving high-dose conditioning with autologous stem cell transplantation.
  • There was no procedure-related mortality and eight patients remained alive 1 year post-transplant.
  • The combination of high-dose EP with melphalan is an active preparative regimen prior to ABMT for hematologic malignancies.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Etoposide / analogs & derivatives. Etoposide / pharmacokinetics. Lymphoma / therapy. Organophosphorus Compounds / pharmacokinetics. Stem Cell Transplantation
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / therapeutic use. Area Under Curve. Chromatography, High Pressure Liquid. Hodgkin Disease / drug therapy. Hodgkin Disease / therapy. Humans. Life Expectancy. Lymphoma, Non-Hodgkin / drug therapy. Lymphoma, Non-Hodgkin / therapy. Melphalan / pharmacokinetics. Middle Aged. Multiple Myeloma / drug therapy. Multiple Myeloma / therapy. Time Factors. Transplantation, Autologous

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  • (PMID = 12692603.001).
  • [ISSN] 0268-3369
  • [Journal-full-title] Bone marrow transplantation
  • [ISO-abbreviation] Bone Marrow Transplant.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-23074; United States / NCI NIH HHS / CA / CA17094; United States / NCI NIH HHS / CA / CA23078
  • [Publication-type] Clinical Trial; Comparative Study; Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organophosphorus Compounds; 528XYJ8L1N / etoposide phosphate; 6PLQ3CP4P3 / Etoposide; Q41OR9510P / Melphalan
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31. DeAngelo DJ, Stone RM: New agents for the treatment of patients with acute lymphoblastic leukemia. Curr Hematol Malig Rep; 2008 Jul;3(3):135-43
Hazardous Substances Data Bank. METHOTREXATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New agents for the treatment of patients with acute lymphoblastic leukemia.
  • Although all patients are treated with similar intensive chemotherapy regimens, good outcomes have occurred more frequently in children than adults.
  • Current adult treatment regimens result in CR rates approaching 80%, with EFS at 5 years of only 30% to 40%.
  • Regardless of age, patients with relapsed or refractory ALL have extremely poor outcomes, because CR rates are low and seldom durable.
  • Clearly, new agents are required to improve the outcome of patients with relapsed or refractory ALL.
  • [MeSH-major] Nucleosides / chemistry. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • [MeSH-minor] Age Factors. Antibodies, Monoclonal / therapeutic use. Asparaginase / chemistry. Asparaginase / therapeutic use. Disease-Free Survival. Enzyme Inhibitors / therapeutic use. HSP90 Heat-Shock Proteins / antagonists & inhibitors. HSP90 Heat-Shock Proteins / metabolism. Humans. Liposomes / chemistry. Liposomes / therapeutic use. Methotrexate / analogs & derivatives. Methotrexate / therapeutic use. Receptors, Notch / antagonists & inhibitors. Receptors, Notch / metabolism. Recurrence

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  • (PMID = 20425458.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Enzyme Inhibitors; 0 / HSP90 Heat-Shock Proteins; 0 / Liposomes; 0 / Nucleosides; 0 / Receptors, Notch; EC 3.5.1.1 / Asparaginase; YL5FZ2Y5U1 / Methotrexate
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32. Mikala G, Jákó J, Vályi-Nagy I: [Proteasome inhibition: a new therapeutic approach for the treatment of multiple myeloma]. Orv Hetil; 2004 Jan 11;145(2):67-74
Hazardous Substances Data Bank. BORTEZOMIB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Proteasome inhibition: a new therapeutic approach for the treatment of multiple myeloma].
  • Multiple myeloma is the second most common hematologic malignancy with currently no definitive treatment available.
  • Although, therapy may include allogenic bone marrow transplantation, high-dose ablative chemotherapy followed by bone marrow or peripheral stem cell transplantation, melphalan/corticosteroid therapy, alpha-interferon treatment, and combined cytostatic chemotherapy, currently none of these alternatives offer cure for the disease.
  • Introduction of thalidomide into the therapeutic arsenal provided a breakthrough in the treatment of refractory and/or relapsing disease, however, clinical experience indicated need for alternative treatments for thalidomide resistant disease as well as for intolerant patients.
  • Proteasome inhibitors, hallmarked by bortezomib may represent one of the much needed therapeutic options.
  • The results of the SUMMIT investigation that involved 202 heavily pretreated patients were convincing enough to prompt the FDA to register this drug for the treatment of multiple myeloma.
  • In this review, the proteasome and its inhibition as a pharmacotherapeutic avenue are introduced.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Enzyme Inhibitors / therapeutic use. Multienzyme Complexes / antagonists & inhibitors. Multiple Myeloma / drug therapy. Multiple Myeloma / enzymology. Pyrazines / therapeutic use
  • [MeSH-minor] Animals. Bortezomib. Clinical Trials, Phase I as Topic. Cysteine Endopeptidases / metabolism. Drug Administration Schedule. Humans. Proteasome Endopeptidase Complex. Randomized Controlled Trials as Topic

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  • (PMID = 14978877.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Enzyme Inhibitors; 0 / Multienzyme Complexes; 0 / Pyrazines; 69G8BD63PP / Bortezomib; EC 3.4.22.- / Cysteine Endopeptidases; EC 3.4.25.1 / Proteasome Endopeptidase Complex
  • [Number-of-references] 23
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33. Williams ME, Densmore JJ: Biology and therapy of mantle cell lymphoma. Curr Opin Oncol; 2005 Sep;17(5):425-31
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biology and therapy of mantle cell lymphoma.
  • Standard and effective treatment approaches have yet to be established.
  • Clinical trials using chemotherapy plus rituximab have shown improved response rates, including complete remissions, but without cure in most cases, indicating a clear need for new treatment approaches.
  • Novel therapies for relapsed disease using the proteasome inhibitor bortezomib, thalidomide plus rituximab, the cyclin inhibitor flavopiridol, or inhibitors of the mammalian target of rapamycin (mTOR) have shown encouraging clinical responses.
  • Stem cell transplantation, including nonmyeloablative approaches, are being incorporated into therapeutic regimens and show promise in both the front-line and relapsed/refractory settings.
  • SUMMARY: This review summarizes recent advances in the biology, pathogenesis, and therapy of mantle cell lymphoma and identifies ongoing areas of clinical investigation and new treatment approaches.
  • [MeSH-major] Biomarkers, Tumor. Lymphoma, Mantle-Cell / physiopathology. Lymphoma, Mantle-Cell / therapy. Stem Cell Transplantation
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Humans. Immunotherapy. Prognosis


34. Lin TS: New agents in chronic lymphocytic leukemia. Curr Hematol Malig Rep; 2010 Jan;5(1):29-34
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Despite advances in treatment, chronic lymphocytic leukemia (CLL) remains incurable with standard therapies.
  • Novel therapeutic agents are needed, particularly for patients with high-risk cytogenetic abnormalities such as del(17p13).
  • The immunomodulatory drug lenalidomide and the cyclin-dependent kinase inhibitor flavopiridol demonstrated clinical activity in fludarabine-refractory CLL patients with high-risk cytogenetic features and bulky lymphadenopathy, but they were associated with toxicities such as tumor flare and tumor lysis.
  • Second-generation monoclonal anti-CD20 antibodies in clinical trials include ofatumumab, which demonstrated activity in fludarabine-refractory patients with bulky lymphadenopathy.
  • Investigational agents with novel therapeutic targets include the anti-CD37 small modular immunopharmaceutical TRU-016, the oral spleen tyrosine kinase (Syk) inhibitor fostamatinib, and the oral phosphatidylinositol-3-kinase (PI3K) inhibitor CAL-101; all of these have all shown preliminary evidence of clinical activity.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drugs, Investigational / therapeutic use. Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Clinical Trials, Phase I as Topic. Clinical Trials, Phase II as Topic. Drug Delivery Systems. Flavonoids / therapeutic use. Humans. Immunologic Factors / therapeutic use. Neoplasm Proteins / antagonists & inhibitors. Piperidines / therapeutic use. Protein Kinase Inhibitors / therapeutic use. Proto-Oncogene Proteins c-bcl-2 / antagonists & inhibitors. Thalidomide / analogs & derivatives. Thalidomide / therapeutic use

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  • (PMID = 20425394.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / Drugs, Investigational; 0 / Flavonoids; 0 / Immunologic Factors; 0 / Neoplasm Proteins; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 45AD6X575G / alvocidib; 4Z8R6ORS6L / Thalidomide; F0P408N6V4 / lenalidomide
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35. Foyil KV, Bartlett NL: Anti-CD30 Antibodies for Hodgkin lymphoma. Curr Hematol Malig Rep; 2010 Jul;5(3):140-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Treatment of refractory or relapsed classical Hodgkin lymphoma (HL) remains challenging, but targeted immunotherapy has recently emerged as a potential treatment option for these patients.
  • Although first-generation monoclonal anti-CD30 antibodies proved disappointing, current efforts to modify anti-CD30 antibodies to improve binding of effector cells and enhance activity appears more promising, as does the development of novel antibody-drug conjugates (ADCs).
  • ADCs offer the potential to deliver potent therapies with minimal toxicity.
  • This article highlights the development of anti-CD30 antibodies and ADCs for relapsed or refractory classical HL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antigens, CD30 / immunology. Antineoplastic Agents / therapeutic use. Hodgkin Disease / drug therapy
  • [MeSH-minor] Clinical Trials as Topic. Humans. Immunoconjugates / therapeutic use. Immunotherapy. Oligopeptides / therapeutic use

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  • (PMID = 20446121.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD30; 0 / Antineoplastic Agents; 0 / Immunoconjugates; 0 / Oligopeptides; 0 / monomethyl auristatin E; 7XL5ISS668 / brentuximab vedotin
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36. Sikder MA, Friedberg JW: Beyond rituximab: The future of monoclonal antibodies in B-cell non-Hodgkin lymphoma. Curr Hematol Malig Rep; 2008 Oct;3(4):187-93
Hazardous Substances Data Bank. RITUXIMAB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The treatment of non-Hodgkin lymphoma (NHL) has changed dramatically since the introduction of rituximab, a monoclonal antibody that binds to the B-cell transmembrane protein CD20 and causes lysis of the lymphoma cells.
  • The goal of these newer agents is to achieve similar or better response rates as seen with rituximab and perhaps demonstrate activity in rituximab-refractory disease.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Lymphoma, B-Cell / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antibodies, Monoclonal, Murine-Derived. Antibodies, Neoplasm / therapeutic use. Clinical Trials as Topic. Humans. Rituximab

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  • (PMID = 20425465.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antibodies, Neoplasm; 0 / Antineoplastic Agents; 0 / PRO131921 monoclonal antibody; 0 / dacetuzumab; 0 / epratuzumab; 0 / ocrelizumab; 0 / veltuzumab; 357613-77-5 / galiximab; 3A189DH42V / alemtuzumab; 4F4X42SYQ6 / Rituximab; M95KG522R0 / ofatumumab
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37. Oki Y, Younes A: Does rituximab have a place in treating classic hodgkin lymphoma? Curr Hematol Malig Rep; 2010 Jul;5(3):135-9
Hazardous Substances Data Bank. VINBLASTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Although this rationale has not generally been confirmed in patients, promising results in managing cHL have occurred in early-phase clinical trials of rituximab, including trials of rituximab as a single agent in refractory or recurrent cHL, rituximab plus gemcitabine in refractory or recurrent cHL, and rituximab plus ABVD in newly diagnosed cHL.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Hodgkin Disease / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal, Murine-Derived. Antigens, CD20 / metabolism. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bleomycin / therapeutic use. Clinical Trials as Topic. Dacarbazine / therapeutic use. Doxorubicin / therapeutic use. Humans. Rituximab. Vinblastine / therapeutic use

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  • (PMID = 20490723.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Antigens, CD20; 0 / Antineoplastic Agents; 11056-06-7 / Bleomycin; 4F4X42SYQ6 / Rituximab; 5V9KLZ54CY / Vinblastine; 7GR28W0FJI / Dacarbazine; 80168379AG / Doxorubicin; ABVD protocol
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38. Mesa RA: New drugs for the treatment of myelofibrosis. Curr Hematol Malig Rep; 2010 Jan;5(1):15-21
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New drugs for the treatment of myelofibrosis.
  • Cure is potentially achievable through allogeneic stem cell transplantation, but this therapy is either inappropriate or not feasible for most patients.
  • MF patients suffer from a range of debilitating disease manifestations (eg, massive splenomegaly, cytopenias, constitutional symptoms, and transformation to a treatment-refractory blast phase).
  • Currently available therapies are palliative but can be of significant value to some MF patients for anemia, splenomegaly, or sometimes both manifestations.
  • New medical therapies for MF revolve around three main themes: immunomodulation (to assist anemia), hypomethylation strategies, and (the most robust pipeline) the use of targeted JAK2 inhibitors.
  • Future targeted agents, and perhaps combinations of agents that currently show complementary benefits, are anticipated to further enhance the efficacy of medical therapy for MF.
  • [MeSH-major] Drugs, Investigational / therapeutic use. Primary Myelofibrosis / drug therapy
  • [MeSH-minor] Anemia / drug therapy. Anemia / etiology. Clinical Trials as Topic. Combined Modality Therapy. DNA Methylation / drug effects. Hematopoietic Stem Cell Transplantation. Humans. Immunologic Factors / therapeutic use. Janus Kinase 2 / antagonists & inhibitors. Janus Kinase 2 / genetics. Palliative Care. Protein Kinase Inhibitors / therapeutic use. Splenomegaly / drug therapy. Splenomegaly / etiology. Thrombocytopenia / drug therapy. Thrombocytopenia / etiology. Treatment Outcome

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  • (PMID = 20425392.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drugs, Investigational; 0 / Immunologic Factors; 0 / Protein Kinase Inhibitors; EC 2.7.10.2 / JAK2 protein, human; EC 2.7.10.2 / Janus Kinase 2
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39. Cavo M: Current status of bortezomib in the treatment of multiple myeloma. Curr Hematol Malig Rep; 2007 May;2(2):128-37
Hazardous Substances Data Bank. BORTEZOMIB .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current status of bortezomib in the treatment of multiple myeloma.
  • Bortezomib (formerly PS-341) has been the first proteasome inhibitor to enter clinical trials in cancer patients.
  • Preclinical studies showing that this novel agent directly inhibits the proliferation of myeloma cells, induces their apoptosis, and abrogates paracrine tumor growth through alteration of interactions of myeloma and stromal cells and through nuclear factor kappaB-dependent cytokine secretion prompted the design of large phase II and III studies of bortezomib in patients with advanced relapsed and/or refractory multiple myeloma.
  • Favorable results of these studies led to accelerated approval for use of bortezomib in patients with multiple myeloma who have progressed after at least their second therapy and, more recently, to expanded approval for second-line use in patients in whom one prior therapy has failed.
  • Combination studies of bortezomib with various agents, including dexamethasone, DNA-damaging drugs (such as melphalan, cyclophosphamide, and doxorubicin), thalidomide, and lenalidomide, are currently ongoing in patients with both relapsed/refractory and newly diagnosed disease.
  • Bortezomib may be the "backbone" for the development of more effective treatment strategies to improve patient outcome in multiple myeloma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Multiple Myeloma / drug therapy. Neoplasm Proteins / antagonists & inhibitors. Protease Inhibitors / therapeutic use. Proteasome Inhibitors. Pyrazines / therapeutic use
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Bortezomib. Cell Line, Tumor / drug effects. Clinical Trials as Topic / statistics & numerical data. Combined Modality Therapy. Cytokines / secretion. Drug Screening Assays, Antitumor. Gene Expression Regulation, Neoplastic / drug effects. Humans. Kidney Failure, Chronic / drug therapy. Kidney Failure, Chronic / etiology. Multicenter Studies as Topic / statistics & numerical data. NF-kappa B / metabolism. Salvage Therapy. Stem Cell Transplantation. Stromal Cells / pathology. Transplantation, Autologous

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  • (PMID = 20425361.001).
  • [ISSN] 1558-822X
  • [Journal-full-title] Current hematologic malignancy reports
  • [ISO-abbreviation] Curr Hematol Malig Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Cytokines; 0 / NF-kappa B; 0 / Neoplasm Proteins; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 50
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40. Shoji N, Ito Y, Kimura Y, Nishimaki J, Kuriyama Y, Tauchi T, Yaguchi M, Payzulla D, Ebihara Y, Ohyashiki K: Pulmonary alveolar proteinosis as a terminal complication in myelodysplastic syndromes: a report of four cases detected on autopsy. Leuk Res; 2002 Jun;26(6):591-5
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  • Secondary pulmonary alveolar proteinosis (PAP) is one of the complications of hematologic malignancy and immunosuppressive diseases.
  • They consisted of two refractory anemia (RA) and two patients with refractory anemia with excess blasts in transformation (RAEBt) at the time of MDS diagnosis, but all of them developed leukemic phase and were resistant to chemotherapy at the time of pulmonary episodes.
  • Previously, 69 patients with PAP associated with hematologic disorders have been reported, but there have been only seven cases with MDS, including our four patients.
  • Of the 69 reported cases of PAP in hematologic malignancies, 24/63 (38%) informative patients with infection had fungal infections of the lung; 2/7 (29%) MDS cases had fungal infection.

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  • [CommentIn] Am J Med. 2003 Dec 1;115(8):674 [14656624.001]
  • (PMID = 12007507.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Number-of-references] 11
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41. Melo JV, Hughes TP, Apperley JF: Chronic myeloid leukemia. Hematology Am Soc Hematol Educ Program; 2003;:132-52
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  • Chronic myeloid leukemia (CML) was the first human malignancy to be associated with a specific genetic lesion, the Philadelphia chromosome, harboring the BCR-ABL oncogene.
  • Since then, it has become a paradigm for the discovery of molecular mechanisms and targeted therapeutic approaches in the field of hematologic neoplasias.
  • In this report, we discuss the biological basis for such translation and highlight the current and potential tools for the effective treatment of CML patients.
  • The first part presents a review of the basic concepts on the biology of CML and their application to the design of targeted therapy.
  • The mechanisms of action of the molecular-specific drugs currently used in clinical trials are discussed, with emphasis on the description of the most promising new compounds that are enhancing the potential for effective alternative or combination chemotherapy in CML.
  • In particular, we discuss the relative value of regular quantitative RT/PCR and cytogenetic analyses, how responding patients should be monitored and managed, and how to investigate patients who are refractory or become resistant to imatinib treatment.
  • We review the current treatment options, highlight the factors impacting on decision making, discuss the range of possibilities for future therapeutic strategies and propose a systematic approach for individualizing treatment for patients in different disease categories.

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  • (PMID = 14633780.001).
  • [ISSN] 1520-4391
  • [Journal-full-title] Hematology. American Society of Hematology. Education Program
  • [ISO-abbreviation] Hematology Am Soc Hematol Educ Program
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / Fusion Proteins, bcr-abl
  • [Number-of-references] 141
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42. Ogasawara T, Yasuyama M, Kawauchi K: Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2). Am J Hematol; 2005 Jun;79(2):136-41
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  • [Title] Therapy-related myelodysplastic syndrome with monosomy 5 after successful treatment of acute myeloid leukemia (M2).
  • We describe a patient who developed myelodysplastic syndrome over 2 years after achieving complete remission of acute myeloid leukemia (AML).
  • The patient was treated in July 1998 with anthracycline, etoposide, and behenoyl cytarabine chemotherapy for AML (French-American-British classification, M2; World Health Organization classification, AML with maturation) and achieved complete remission.
  • The patient was diagnosed with high-grade myelodysplastic syndrome (MDS)/refractory anemia with excess blasts (RAEB) subtype.
  • Therapy-related MDS and AML (t-MDS/t-AML) developing after treatment for acute leukemia is unusual; the primary leukemia associated with most cases of t-MDS/t-AML is acute promyelocytic leukemia (APL).
  • This unusual case suggests that AML excluding APL should be considered a primary hematologic malignancy for t-MDS/t-AML.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Chromosomes, Human, Pair 5. Cytarabine / analogs & derivatives. Leukemia, Myeloid, Acute / chemically induced. Monosomy. Myelodysplastic Syndromes / chemically induced. Myelodysplastic Syndromes / genetics


43. Browning CE, Dixon JE, Malone JC, Callen JP: Thalidomide in the treatment of recalcitrant Sweet's syndrome associated with myelodysplasia. J Am Acad Dermatol; 2005 Aug;53(2 Suppl 1):S135-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Thalidomide in the treatment of recalcitrant Sweet's syndrome associated with myelodysplasia.
  • Sweet's syndrome is a neutrophilic dermatosis characterized by tender, erythematous, pseudovesicular plaques that can be associated with hematologic malignancy.
  • The delay between the onset of Sweet's syndrome and the subsequent diagnosis of myelodysplasia highlights the need for thorough and repeated evaluation for underlying malignancy in patients with such a course.
  • Although corticosteroids are the initial treatment of choice, this patient's eruption was only partially responsive to high-dose prednisone and was refractory to metronidazole, dapsone, and methotrexate.
  • Treatment with thalidomide resulted in complete resolution of the cutaneous lesions within one month of therapy.
  • [MeSH-major] Immunosuppressive Agents / therapeutic use. Myelodysplastic Syndromes / complications. Myelodysplastic Syndromes / drug therapy. Sweet Syndrome / complications. Sweet Syndrome / drug therapy. Thalidomide / therapeutic use

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  • (PMID = 16021163.001).
  • [ISSN] 1097-6787
  • [Journal-full-title] Journal of the American Academy of Dermatology
  • [ISO-abbreviation] J. Am. Acad. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 4Z8R6ORS6L / Thalidomide
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44. Wahl RL: Tositumomab and (131)I therapy in non-Hodgkin's lymphoma. J Nucl Med; 2005 Jan;46 Suppl 1:128S-40S
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tositumomab and (131)I therapy in non-Hodgkin's lymphoma.
  • Currently, it is approved for use in patients whose disease has relapsed after chemotherapy and is refactory to rituximab, including patients whose tumors have transformed to a higher histologic grade.
  • This review outlines the current and evolving status of this therapeutic regimen at nonmyeloablative doses.
  • METHODS: Clinical data from multiple published studies and preliminary communications encompassing more than 1,000 patients were reviewed to describe the current status of tositumomab and (131)I-tositumomab therapy.
  • The therapy is delivered in 2 parts, a dosimetric dose and a therapeutic dose.
  • The therapeutic radioactivity millicurie dose is calculated on a patient-individualized ("tailored") basis.
  • A series of 3 total-body gamma-camera scans are used to determine the patient-specific pharmacokinetics (total-body residence time) of the radiolabeled antibody conjugate required to deliver the desired total-body radiation dose, typically 75 cGy.
  • RESULTS: In clinical trials, objective response rates in patients who had been extensively pretreated with chemotherapy ranged from 47% to 68%.
  • Tositumomab and (131)I-tositumomab therapy also was effective in patients who had failed to respond to or who had relapsed after rituximab therapy, with a 68% overall response rate.
  • Single-center trials using tositumomab and (131)I-tositumomab therapy alone or after chemotherapy in previously untreated patients have shown response rates in excess of 90%, with most responses complete.
  • Toxicity is predominately hematologic; however, human antimouse antibodies, hypothyroidism, and myelodysplastic syndrome have been reported in a small fraction of patients.
  • CONCLUSION: Tositumomab and (131)I-tositumomab therapy at patient-specific, nonmyeloablative doses is safe and effective in treatment of relapsed and refractory follicular NHL.
  • Toxicity is mainly hematologic and reversible.
  • Tositumomab and (131)I-tositumomab therapy is assuming a growing role in this common malignancy.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Clinical Trials as Topic. Lymphoma, Non-Hodgkin / radiotherapy. Radioimmunotherapy / methods
  • [MeSH-minor] Animals. Humans. Immunotherapy / methods. Practice Guidelines as Topic. Practice Patterns, Physicians'. Treatment Outcome

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  • (PMID = 15653661.001).
  • [ISSN] 0161-5505
  • [Journal-full-title] Journal of nuclear medicine : official publication, Society of Nuclear Medicine
  • [ISO-abbreviation] J. Nucl. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / iodine-131 anti-B1 antibody
  • [Number-of-references] 49
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45. Sjak-Shie NN, Vescio RA, Berenson JR: Recent advances in multiple myeloma. Curr Opin Hematol; 2000 Jul;7(4):241-6
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  • Multiple myeloma is the second most common hematologic malignancy, with approximately 15,000 new cases each year in the United States.
  • The roles of cytogenetic abnormalities as well as aberrant angiogenesis and cytokine expression in the etiology of myeloma continue to be explored and may lead to future therapeutic strategies.
  • Finally, thalidomide offers significant clinical benefit to patients with myeloma previously refractory to multiple agents, and its role in early stages of the disease is under investigation.
  • [MeSH-major] Multiple Myeloma / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bone Marrow / pathology. Bone Marrow / virology. Bone Marrow Transplantation. Chromosome Aberrations. Combined Modality Therapy. Cytokines / physiology. Diphosphonates / therapeutic use. Growth Substances / physiology. Hematopoietic Stem Cell Transplantation. Herpesviridae Infections / complications. Herpesviridae Infections / diagnosis. Herpesvirus 8, Human / isolation & purification. Herpesvirus 8, Human / pathogenicity. Humans. Neoplasm Proteins / physiology. Neovascularization, Pathologic. Osteolysis / drug therapy. Osteolysis / etiology. Osteolysis / radiotherapy. Plasma Cells / pathology. Remission Induction. Salvage Therapy. Thalidomide / therapeutic use

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  • (PMID = 10882180.001).
  • [ISSN] 1065-6251
  • [Journal-full-title] Current opinion in hematology
  • [ISO-abbreviation] Curr. Opin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Cytokines; 0 / Diphosphonates; 0 / Growth Substances; 0 / Neoplasm Proteins; 4Z8R6ORS6L / Thalidomide
  • [Number-of-references] 75
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46. Berkers CR, Verdoes M, Lichtman E, Fiebiger E, Kessler BM, Anderson KC, Ploegh HL, Ovaa H, Galardy PJ: Activity probe for in vivo profiling of the specificity of proteasome inhibitor bortezomib. Nat Methods; 2005 May;2(5):357-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Proteasome inhibitors, such as the dipeptide boronic acid bortezomib, are emerging as important tools in the treatment of the fatal hematologic malignancy multiple myeloma.
  • Despite the recent US Food and Drug Administration approval of bortezomib (PS341, Velcade) for the treatment of refractory multiple myeloma, many of the basic pharmacologic parameters of bortezomib and its mode of action on myeloma cells remain to be determined.
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Bortezomib. Cell Line, Tumor / drug effects. Humans. Leupeptins / pharmacology. Mice. Multiple Myeloma / drug therapy. Proteasome Endopeptidase Complex / pharmacology

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  • (PMID = 15846363.001).
  • [ISSN] 1548-7091
  • [Journal-full-title] Nature methods
  • [ISO-abbreviation] Nat. Methods
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Leupeptins; 0 / Protease Inhibitors; 0 / Pyrazines; 133407-82-6 / benzyloxycarbonylleucyl-leucyl-leucine aldehyde; 69G8BD63PP / Bortezomib; EC 3.4.25.1 / Proteasome Endopeptidase Complex
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47. Richardson PG, Hideshima T, Anderson KC: Bortezomib (PS-341): a novel, first-in-class proteasome inhibitor for the treatment of multiple myeloma and other cancers. Cancer Control; 2003 Sep-Oct;10(5):361-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bortezomib (PS-341): a novel, first-in-class proteasome inhibitor for the treatment of multiple myeloma and other cancers.
  • BACKGROUND: Multiple myeloma (MM) is an incurable malignancy that is diagnosed in approximately 15,000 people in the United States each year.
  • We also address the potential for bortezomib as a therapy for MM.
  • CONCLUSIONS: Proteasome inhibition is a promising new investigational avenue for cancer therapy.
  • Bortezomib is currently available for the treatment of relapsed and refractory MM.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Boronic Acids / therapeutic use. Multiple Myeloma / drug therapy. Protease Inhibitors / therapeutic use. Pyrazines / therapeutic use

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  • (PMID = 14581890.001).
  • [ISSN] 1073-2748
  • [Journal-full-title] Cancer control : journal of the Moffitt Cancer Center
  • [ISO-abbreviation] Cancer Control
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Boronic Acids; 0 / Protease Inhibitors; 0 / Pyrazines; 69G8BD63PP / Bortezomib
  • [Number-of-references] 48
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48. Rojnuckarin P, Nakorn TN, Assanasen T, Wannakrairot P, Intragumtornchai T: Cyclosporin in subcutaneous panniculitis-like T-cell lymphoma. Leuk Lymphoma; 2007 Mar;48(3):560-3
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  • Subcutaneous panniculitis-like T-cell lymphoma (SPTCL) is a rare form of hematologic malignancy characterized by lesions in subcutaneous fat associated with systemic symptoms.
  • The standard treatment of the disease, currently, is not established, but CHOP or CHOP-like regimens are usually given.
  • We report, herein, 4 cases of SPTCL diagnosed by histopathology and immunohistochemistry who were refractory to CHOP and/or ESHAP and/or fludarabine-based regimen, but showed rapid improvement within weeks after oral cyclosporin 4 mg/kg/day.
  • Three sustained complete remission for the durations of 8 - 9 months off-treatments.
  • Our data suggest the benefit of incorporating cyclosporin into the treatment regimen for SPTCL.
  • [MeSH-major] Cyclosporine / therapeutic use. Immunosuppressive Agents / therapeutic use. Lymphoma, T-Cell, Cutaneous / drug therapy. Panniculitis / pathology. Skin Neoplasms / drug therapy
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / therapeutic use. Cyclophosphamide / therapeutic use. Cytarabine / therapeutic use. Doxorubicin / therapeutic use. Etoposide / therapeutic use. Female. Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor. Humans. Male. Methylprednisolone / therapeutic use. Middle Aged. Prednisone / therapeutic use. Prognosis. Remission Induction. Treatment Outcome. Vincristine / therapeutic use

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  • (PMID = 17454599.001).
  • [ISSN] 1042-8194
  • [Journal-full-title] Leukemia & lymphoma
  • [ISO-abbreviation] Leuk. Lymphoma
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 04079A1RDZ / Cytarabine; 5J49Q6B70F / Vincristine; 6PLQ3CP4P3 / Etoposide; 80168379AG / Doxorubicin; 83HN0GTJ6D / Cyclosporine; 8N3DW7272P / Cyclophosphamide; Q20Q21Q62J / Cisplatin; VB0R961HZT / Prednisone; X4W7ZR7023 / Methylprednisolone; CHOP protocol; ESAP protocol
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49. Richardson P, Mitsiades C, Laubach J, Schlossman R, Ghobrial I, Hideshima T, Munshi N, Anderson K: Lenalidomide in multiple myeloma: an evidence-based review of its role in therapy. Core Evid; 2009;4:215-45

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lenalidomide in multiple myeloma: an evidence-based review of its role in therapy.
  • INTRODUCTION: Multiple myeloma (MM) is a relatively common and incurable hematological malignancy.
  • Currently, there is no single standard therapy, with choice of treatment dependent on individual patient factors.
  • Lenalidomide is an immunomodulatory drug with potent antitumor, antiangiogenic, immunomodulatory, and proapoptotic activity in MM.
  • AIMS: To evaluate the evidence for the use of lenalidomide in its current indication in relapsed or refractory MM, and additionally its investigational use for the treatment of newly diagnosed MM.
  • EVIDENCE REVIEW: In patients with relapsed and refractory MM, adding lenalidomide to high-dose dexamethasone significantly improves response rates and time-to-progression, relative to high-dose dexamethasone alone.
  • Outcome is independent of patient age, number of previous therapies, type of previous therapy (including thalidomide or autologous stem cell transplantation), renal impairment, and beta(2)-microglobulin level.
  • Myelosuppression is the predominant toxicity observed, although some studies have shown high incidences of venous thromboembolism in the absence of prophylactic antithrombotic anticoagulation therapy.
  • ROLE IN THERAPY: The encouraging results obtained with lenalidomide alone and in combination with dexamethasone in patients with relapsed or refractory MM have led to its adoption as a recommended therapy in patients who have received at least one prior treatment.
  • Emerging evidence supports the ongoing investigation of lenalidomide in combination with low-dose dexamethasone, and in other combinations including bortezomib, for use both in relapsed, refractory, and newly diagnosed MM.

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  • (PMID = 20694078.001).
  • [ISSN] 1555-175X
  • [Journal-full-title] Core evidence
  • [ISO-abbreviation] Core Evid
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Other-IDs] NLM/ PMC2899783
  • [Keywords] NOTNLM ; evidence / lenalidomide / multiple myeloma / outcomes / treatment
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50. Hoelzer D, Gökbuget N, Ottmann OG: Targeted therapies in the treatment of Philadelphia chromosome-positive acute lymphoblastic leukemia. Semin Hematol; 2002 Oct;39(4 Suppl 3):32-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted therapies in the treatment of Philadelphia chromosome-positive acute lymphoblastic leukemia.
  • Imatinib mesylate (Gleevec, Novartis Pharmaceuticals Corp, East Hanover, NJ; Glivec, Novartis Pharma AG, Basel, Switzerland), a signal transduction inhibitor with preferential effects against the tyrosine kinase activity of the protein product of the ABL proto-oncogene, induced hematologic responses in >or=90% of patients with chronic-phase chronic myeloid leukemia (CML).
  • In Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL), the BCR-ABL translocation is the main transforming event, making it another hematologic malignancy targeted by this ABL-tyrosine kinase inhibitor.
  • In an international multicenter phase II trial, imatinib-induced hematologic responses (typically brief) were achieved in 60% of patients with relapsed or refractory Ph(+) ALL.
  • Subsequently, the German Multicenter Study Group for Adult ALL (GMALL) analyzed 59 patients treated in two successive nonrandomized phase II trials of imatinib in patients with relapsed or refractory Ph(+) ALL.
  • However, in a significant proportion, blast counts subsequently increased 16 to 50 days after treatment onset.
  • Rapid development of resistance during treatment with imatinib mesylate remains a major problem.
  • Further research efforts should explore the mechanisms of resistance to imatinib mesylate; effectiveness of other targeted therapies (eg, farnesyl transferase inhibitors [FTIs]); combination therapies; and inclusion of strategies for immune response modification (eg, donor lymphocyte infusions, interferon-alpha) for Ph/BCR-ABL-positive leukemias.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Piperazines / therapeutic use. Precursor Cell Lymphoblastic Leukemia-Lymphoma / drug therapy. Pyrimidines / therapeutic use
  • [MeSH-minor] Benzamides. Drug Resistance, Neoplasm. Humans. Imatinib Mesylate. Neoplasm, Residual. Treatment Outcome

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  • [Copyright] Copyright 2002, Elsevier Science (USA). All rights reserved.
  • (PMID = 12447850.001).
  • [ISSN] 0037-1963
  • [Journal-full-title] Seminars in hematology
  • [ISO-abbreviation] Semin. Hematol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Piperazines; 0 / Pyrimidines; 8A1O1M485B / Imatinib Mesylate
  • [Number-of-references] 23
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51. Rajkumar SV, Gertz MA, Kyle RA, Greipp PR, Mayo Clinic Myeloma, Amyloid, and Dysproteinemia Group: Current therapy for multiple myeloma. Mayo Clin Proc; 2002 Aug;77(8):813-22
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current therapy for multiple myeloma.
  • Multiple myeloma is an incurable plasma cell malignancy that accounts for 10% of all hematologic cancers.
  • For decades the mainstay of therapy has been the use of melphalan and prednisone; with this regimen, the median survival is approximately 3 years.
  • Because of the increasing use of transplantation as initial therapy, several therapeutic issues have emerged: the role of tandem transplantation, early vs delayed transplantation, and the role of allogeneic transplantation.
  • The pronounced activity of thalidomide in patients with refractory myeloma represents another important advance.
  • This has prompted the study of several novel agents in the treatment of myeloma, at least 2 of which appear promising.
  • The purpose of this review is to summarize recent advances and provide an evidence-based approach to the treatment of multiple myeloma.
  • [MeSH-major] Multiple Myeloma / therapy
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy. Drug Therapy, Combination. Glucocorticoids / therapeutic use. Hematopoietic Stem Cell Transplantation. Humans. Immunosuppressive Agents / therapeutic use. Recurrence. Thalidomide / therapeutic use

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  • [CommentIn] Mayo Clin Proc. 2002 Dec;77(12):1395; author reply 1395 [12479531.001]
  • [CommentIn] Mayo Clin Proc. 2003 Jan;78(1):118; author reply 118 [12528887.001]
  • (PMID = 12173715.001).
  • [ISSN] 0025-6196
  • [Journal-full-title] Mayo Clinic proceedings
  • [ISO-abbreviation] Mayo Clin. Proc.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA62242; United States / NCI NIH HHS / CA / CA85818; United States / NCI NIH HHS / CA / CA93842
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / Immunosuppressive Agents; 4Z8R6ORS6L / Thalidomide
  • [Number-of-references] 89
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52. Devizzi L, Guidetti A, Tarella C, Magni M, Matteucci P, Seregni E, Chiesa C, Bombardieri E, Di Nicola M, Carlo-Stella C, Gianni AM: High-dose yttrium-90-ibritumomab tiuxetan with tandem stem-cell reinfusion: an outpatient preparative regimen for autologous hematopoietic cell transplantation. J Clin Oncol; 2008 Nov 10;26(32):5175-82
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: To develop high-dose myeloablative therapy for CD20(+) non-Hodgkin's lymphoma (NHL) as a safe and widely applicable regimen.
  • PATIENTS AND METHODS: Patients with relapsed/refractory (n = 25) or de novo high-risk (n = 5) NHL received one myeloablative dose of yttrium-90 ((90)Y)-ibritumomab tiuxetan after five chemotherapy courses, including three cycles of anthracycline- or platinum-containing regimens, one cycle of cyclophosphamide (4 to 7 g/m(2)), and one cycle of cytarabine (12 to 24 g/m(2)).
  • To minimize hematologic toxicity, stem cells were reinfused at days 7 and 14 after (90)Y-ibritumomab tiuxetan.
  • Hematologic toxicity was mild to moderate and of short duration.
  • After a median observation time of 30 months (range, 22 to 48 months), no myeloid secondary malignancy or chromosomal abnormality was observed, the OS rate was 87%, and the EFS rate was 69%.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Hematopoietic Stem Cell Transplantation. Lymphoma, Non-Hodgkin / radiotherapy. Radioimmunotherapy
  • [MeSH-minor] Adult. Aged. Ambulatory Care. Antigens, CD20 / analysis. Chemotherapy, Adjuvant. Cytogenetic Analysis. Disease-Free Survival. Female. Humans. Male. Middle Aged. Neoplasm Staging. Radiotherapy Dosage. Radiotherapy, Adjuvant. Time Factors. Transplantation, Autologous. Treatment Outcome

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  • [CommentIn] J Clin Oncol. 2009 Mar 1;27(7):1145-6; author reply 1146 [19171699.001]
  • [CommentIn] J Clin Oncol. 2008 Nov 10;26(32):5147-50 [18854559.001]
  • (PMID = 18854569.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, CD20; 0 / ibritumomab tiuxetan
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53. Saccaro S, Fonseca R, Veillon DM, Cotelingam J, Nordberg ML, Bredeson C, Glass J, Munker R: Primary plasma cell leukemia: report of 17 new cases treated with autologous or allogeneic stem-cell transplantation and review of the literature. Am J Hematol; 2005 Apr;78(4):288-94
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary plasma cell leukemia (PPCL) is a rare hematologic malignancy characterized by the proliferation of plasma cells in blood, bone marrow, and other organs in the absence of established multiple myeloma.
  • PPCL has a poor prognosis when treated with conventional therapy for multiple myeloma.
  • He was treated with hyper-CVAD, entered complete remission, and then proceeded to high-dose chemotherapy with peripheral stem-cell support.
  • He was treated with VAD chemotherapy and underwent allogeneic bone marrow transplantation from his HLA-identical sister.
  • He remained in complete remission for 3 years and then developed progressive refractory disease, dying 7 years after the initial diagnosis.
  • Finally, the features of PPCL, the outcome, published data of SCT for PPCL, and indications for treatment are discussed.
  • [MeSH-major] Leukemia, Plasma Cell / therapy. Stem Cell Transplantation
  • [MeSH-minor] Adult. Humans. Male. Middle Aged. Prognosis. Transplantation, Autologous. Transplantation, Homologous. Treatment Outcome

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  • (PMID = 15795922.001).
  • [ISSN] 0361-8609
  • [Journal-full-title] American journal of hematology
  • [ISO-abbreviation] Am. J. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 37
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54. Leitman SF, Tisdale JF, Bolan CD, Popovsky MA, Klippel JH, Balow JE, Boumpas DT, Illei GG: Transfusion-associated GVHD after fludarabine therapy in a patient with systemic lupus erythematosus. Transfusion; 2003 Dec;43(12):1667-71
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transfusion-associated GVHD after fludarabine therapy in a patient with systemic lupus erythematosus.
  • BACKGROUND: Fludarabine, a purine antimetabolite with potent immunosuppressive properties, has previously been associated with the development of transfusion-associated GVHD (TA-GVHD) in patients with hematologic malignancies.
  • STUDY DESIGN AND METHODS: A 42-year-old female with refractory lupus nephritis received three monthly cycles of fludarabine (30 mg/m2/day on Days 1-3) and cyclophosphamide (500 mg/m2 on Day 1).
  • Two weeks later, fever, rash, aminotransferase elevations, hyperbilirubinemia, and pancytopenia developed.
  • Treatment with antithymocyte globulin, cyclosporine, and prednisone was followed by preparatory conditioning for a PBPC transplant from an HLA-identical sibling, but the patient died of disseminated candidiasis before transplant.
  • CONCLUSIONS: Fludarabine and other purine analogs are increasingly used in the treatment of disorders other than hematologic malignancy, such as autoimmune disease.
  • The occurence of TA-GVHD after fludarabine therapy in a patient with lupus strongly suggests that this drug is sufficiently immunoablative to be an independent risk factor for TA-GVHD.
  • Irradiation of blood components should be considered in all patients who receive fludarabine therapy.
  • [MeSH-major] Erythrocyte Transfusion / adverse effects. Graft vs Host Disease / etiology. Immunosuppressive Agents / adverse effects. Lupus Erythematosus, Systemic / drug therapy. Platelet Transfusion / adverse effects. Vidarabine / adverse effects. Vidarabine / analogs & derivatives
  • [MeSH-minor] Adult. Cyclophosphamide / adverse effects. Drug Therapy, Combination. Fatal Outcome. Female. Histocompatibility Testing. Humans. Risk Factors

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  • [CommentIn] Transfusion. 2003 Dec;43(12):1652-4 [14641857.001]
  • [CommentIn] Transfusion. 2003 Dec;43(12):1655-7 [14641858.001]
  • (PMID = 14641861.001).
  • [ISSN] 0041-1132
  • [Journal-full-title] Transfusion
  • [ISO-abbreviation] Transfusion
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 8N3DW7272P / Cyclophosphamide; FA2DM6879K / Vidarabine; P2K93U8740 / fludarabine
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55. Besa EC, Kim PW, Haurani FI: Treatment of primary defective iron-reutilization syndrome: revisited. Ann Hematol; 2000 Aug;79(8):465-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment of primary defective iron-reutilization syndrome: revisited.
  • We encountered two patients who presented with hypochromic-microcytic anemia and were refractory to iron therapy.
  • The hematologic picture consisted of hypochromic-microcytic anemia, low serum iron, low to normal iron binding capacity, high serum ferritin, and increased bone marrow iron in the absence of ringed sideroblasts.
  • These patients had symptomatic anemia and received danazol (200 mg orally) three times per day to which they responded very well with an increase of approximately 3 g in the hemoglobin concentration over 1 year and amelioration of their symptoms.
  • In the differential diagnosis of hypochromic-microcytic anemia, especially in postmenopausal women, one has to consider this type of treatable anemia when more common types such as iron deficiency, chronic inflammation, malignancy, sideroblastic anemia, or thalassemia have been ruled out.
  • [MeSH-major] Anemia, Iron-Deficiency / drug therapy
  • [MeSH-minor] Aged. Cohort Studies. Danazol / therapeutic use. Estrogen Antagonists / therapeutic use. Female. Humans. Iron / metabolism. Middle Aged

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  • (PMID = 10985370.001).
  • [ISSN] 0939-5555
  • [Journal-full-title] Annals of hematology
  • [ISO-abbreviation] Ann. Hematol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Estrogen Antagonists; E1UOL152H7 / Iron; N29QWW3BUO / Danazol
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